Home » Alzheimer’s as a viral infection? The neurologist Rossini: “It is not a communicable disease”

Alzheimer’s as a viral infection? The neurologist Rossini: “It is not a communicable disease”

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Alzheimer’s as a viral infection?  The neurologist Rossini: “It is not a communicable disease”

Can Alzheimer’s be transmitted from person to person or through medications? This is the question that has been circulating online in recent hours following the publication of a study in the scientific journal Nature Medicine then also taken up by the Guardian and the Times which tells of five cases of Alzheimer’s linked to taking a drug and led researchers to hypothesize that the disease is potentially transmissible.

Treatment with cadaveric growth hormones

Researchers at the Prion Disease Research Institute at University College London noted that between 1959 and 1985 at least 1,848 people in Britain were treated with growth hormone extracted from the pituitary gland of corpses, a withdrawn product. worldwide following consignments contaminated with infectious agents (prions) of Creutzfeldt-Jakob disease, known as ‘mad cow disease’.

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Research

The newly published study analyzed the cases of eight people in Great Britain who had been treated with growth hormone in childhood and who had not developed Creutzfeldt-Jakob disease. Of these, five aged between 33 and 55 showed symptoms of early dementia, compatible with Alzheimer’s disease, two had mild symptoms and the third was asymptomatic.

Even if these are few cases, one might be led to think that Alzheimer’s disease could be acquired through taking drugs and is potentially transmissible. “Actually – he clarifies Paolo Maria Rossinidirector of the Department of Neuroscience and Neurorehabilitation of the Irccs San Raffaele Rome – the study suggests the possibility that in drugs derived from animal organisms there could be contaminants (viruses or parts of them such as prions) capable of inducing neurodegeneration and dementia “.

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The French ‘small epidemic’

It had already happened in the past, for example in France, that drugs containing derivatives from human pituitary glands of subjects suffering from Creutzfeld-Jakob dementia (similar to ‘mad cow disease and caused by prions) had induced a ‘small epidemic of this form of dementia for which this production was immediately interrupted. But since many years pass between administration and the development of the disease, the number of patients treated had grown significantly in the meantime.

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Early onset of dementia

“In this study however – adds Rossini – there is a completely new result on which John Collinge’s group has been working for years and that is that subjects treated with derivatives from animal organisms for dwarfism do not develop Jakob’s syndrome after many years -Creutzfeldt, but a form of dementia with typical characteristics of Alzheimer’s including the presence of beta-amyloid plaques and neurofibrillary tangles of tau protein with very early onset, well before the age of 50. Obviously this is very interesting and also worrying because while the annual number of ‘mad cow’ type dementias in our country is a few dozen cases a year, Alzheimer’s type dementias have tens of thousands of new cases every year for a total that is currently around 50% of all cases of dementia in Italy, i.e. well over 500,000 units”.

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Is Alzheimer’s a communicable disease?

Although growth hormone is no longer used, researchers underline the need for strong attention to the risk of possible transmission carried by pharmacological treatments. “In extraordinary circumstances – the neurologists commented in Nature Medicine Mathias Jucker e Lary C. Walker from the German University of Tübingen – Alzheimer’s disease could be transmitted by a mechanism similar to that of prion transmission”.

Is there really a possibility that Alzheimer’s is transmissible? “This hypothesis is not new and comes back into fashion cyclically, but it has never received confirmation in recent decades from any of the research carried out on humans, especially post-mortem, that is, on the brains of subjects who died due to Alzheimer’s, in which direct or indirect prion derivatives have never been detected with certainty”, replies Rossini.

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Prions as ‘extras’ in the genesis of dementia

The problem is that this disease (as well as other forms of dementia) has a very long ‘incubation’ period. “Over the years – continues the neurologist – neurodegenerative mechanisms attack and successively destroy synapses, connections and finally nerve cells without however manifesting themselves clinically”. In other words, the attacked subjects are perfectly normal thanks to the amount of neural and cognitive reserve with which each of us is genetically endowed and which continues to develop throughout life, a reserve that becomes very useful during the aging of the brain.

So? “It could be – Rossini continues – that the prions participate only in the first phases, and then disappear, in which the processes of alteration of the metabolism of the proteins involved are activated and which first lead to the formation of amyloid which does not dissolve, but progressively aggregates in fibrils and then in plaques and subsequently to that of neurofibrillary tangles that ‘suffocate’ the attacked neurons from the inside. In other words, they could be ‘extras’ that surround the ‘first actors, playing some role which, however, I don’t think is generalizable to the most widespread form of Alzheimer’s”.

Alzheimer’s is not an infection

It is also reassuring John Collingeco-author of the study and director of England’s UCL Institute of Prion Diseases, who said: “We are not suggesting that you can ‘get’ Alzheimer’s disease. It is not as transmissible as a viral or bacterial infection.”

Regardless of this study, is there any basis for the idea that Alzheimer’s is contagious? “It has never been demonstrated in the classic sense of the term ‘contagion’, that is, the passage from one being to another through contact or sharing of biological substances, for example breath droplets as in Covid and I am not aware of any studies that demonstrate particular concentrations of cases in some places compared to others in a convincing way. It is a recurring hypothesis that decays for some time and then ‘resurrects’ in the light of some new study. I frankly do not believe, however, that the 5 cases described represent a contingent of any significance compared to the millions of cases present even in the same country as the researchers”.

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New perspectives for research?

Even if the reported cases are few and concern a therapy that is no longer available, this study could open new perspectives for Alzheimer’s research. “It is difficult to think that useful ideas for therapeutic developments could emerge from this work. Certainly in light of what has emerged so far, greater attention will have to be paid to the procedures for detecting/eliminating/sterilizing inoculated or ingested substances and surgical instruments”, he warns Rossini.

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